# su18: see qs2 # su-: see su( ) # Su-: see Su( ) # Su-Pm: see Su(bwV1) # sus-pr: see In(3R)su(pr) # Su-x4: see Su(sph) #*su(b): suppressor of black location: 1-0.1. origin: Spontaneous. discoverer: Plough, 23j28. references: 1927, Proc. Intern. Congr. Genet., 5th., Vol. 2: 1193-1200. Sherald, 1981, Mol. Gen. Genet. 183: 102-06. phenotype: Suppresses b so that body color is only slightly darker than wild type. No dominant effect. Causes the level of |-alanine, which is ordinarily reduced, to return to normal in b/b flies; su(b)6 in b+ genotypes leads to 60% increase above normal |-alanine levels. su(b)6 flies are unable to survive on 0.2 M |-alanine; apparently |-alanine ingested by females prevents su(b) embryos from hatching or the unhatched embryos from melanizing (Campbell and Sherald, 1987, DIS 66: 34). Also effects a return to normal of the fine struc- ture of the puparial case in su(b)6; b/b individuals. alleles: allele origin discoverer synonym ref ( comments ___________________________________________________________________ su(b)1 spont Plough, 1 frequently reverts 23j28 fertility reduced su(b)2 EMS Sherald su(b)11 2 complements su(b)4 su(b)3 EMS Sherald su(b)12 2 reisolate of su(b)2? su(b)4 EMS Sherald su(b)13 2 complements su(b)2 su(b)5 EMS Sherald su(b)14 2 reisolate of su(b)2? su(b)6 EMS Sherald su(b)31 2 non complementing su(b)7 EMS Kolbak su(b)DK ? 3 su(b)8 EMS Kolbak 3 su(b)9 EMS Kolbak 3 su(b)10 EMS Kolbak 3 su(b)11 EMS Kolbak 3 su(b)12 EMS Kolbak 3 ( 1 = Plough, 1927, Proc. Intern. Congr. Genet., 5th., Vol. 2: 1193-1200; 2 = Sherald, 1981, Mol. Gen. Genet. 183: 102-06; 3 = S/ndergaard and Kolbak, 1987, DIS 66: 134. cytology: Placed in 1B4-9 based on its being covered by the terminal deficiency, Df(1)260-1 = Df(1)1A4-6 but not by Df(1)yT4-12 = Df(1)1A7-9 (Sherald and Voelker, 1985, DIS 61: 155). # Su(b): Suppressor of black location: 1-55.5 [1-2 X 10-4 units distal to the distal end of the r locus; possibly a regulatory sequence (S/ndergaard and Kolbak, 1987, DIS 66: 134)]. references: Pedersen, 1982, Carlsberg Res. Commun. 47: 391- 400. phenotype: A semidominant suppressor of b; homozygotes and hem- izygotes in combination with b are slightly darker than wild type, whereas heterozygotes are intermediate between b and wild type in cuticle reflectance. Su(b) by itself has no visible phenotype. Although supplementation of the medium with 6-azathymine, an inhibitor of dihydrouracil dehydro- genase, results in a dark body color in wild-type flies, it does not darken the wild-type coloration of Su(b); b. The double-mutant combination, Su(b) r, does not suppress b (Bahn and S/ndergaard, 1983, Hereditas 99: 309-10), whereas su(r) Su(b); b flies have enhanced black cuticle. Unlike su(b); b, the combination Su(b); b is not sensitive to dietary |-alanine (Campbell and Sherald, 1987, DIS 66: 34). cytology: Placed in 15A1 based on its virtual inseparability from r. #*su(B): suppressor of Bar location: 2-94. origin: Spontaneous. discoverer: Steinberg, 36l. synonym: m(B): modifier of Bar. references: 1937, DIS 7: 20. 1937, DIS 8: 11. 1939, DIS 12: 49. 1940, Collecting Net 15: 173. 1941, Genetics 26: 325-46, 440-51. phenotype: When homozygous, increases number of eye facets from about 75 to 220 in B male and to 140 in B/B female. Affects all B effects but not ey2 or wild type. RK2. #*su(B)2: suppressor of Bar in chromosome 2 location: 2-46 or -60 (7 units from Tft). origin: Spontaneous. discoverer: Gans. phenotype: su(B)2/su(B)2 causes B/+ female to appear wild type. RK2. #*su(B)4: suppressor of Bar in chromosome 4 location: 4- (not located). origin: Spontaneous. discoverer: Brehme, 39k. synonym: m(B)4: modifier of Bar in chromosome 4. references: 1942, DIS 16: 47. phenotype: Facet number in eyes of B male increased, approach- ing that of B/+ female. Effect increases with age of culture. B/B and B/+ female not affected. RK3. # Su(bwV1): Suppressor of brown-Variegated location: 2-105.2. origin: Spontaneous. discoverer: Kadel, 59b17. synonym: Su-Pm: Suppressor of Plum. references: 1959, DIS 33: 95. phenotype: Su(bwV1)/bwV1 has wild-type eye color with peppering of dark spots instead of the more or less uniform brown of bwV1/+. Effect on various bwV chromosomes varies from none for some to complete suppression for others. Pteridines of heads of bwD/bw Su(bwVI) heterozygotes increased to 28% of normal from 2.5% for bwD/+ heterozygotes (Henikoff and Dreesen). Homozygous viable. RK2. cytology: No gross aberration (Lindsley). In situ hybridiza- tion using bw cDNA probe shows a tandem duplication of the sequence, possibly including 59E2-F1 (Dreesen and Henikoff). other information: Su(bwVI) is a tandem duplication of bw+ and flanking sequences based on wild-type phenotype of bw/bw Su(bwVI) and bw5/bw5 Su(bwVI) (Kadel and Wright). Homozygous Su(bwV1) female produces 0.3% reversions associated with crossing over in a manner analogous to reversions of B. # su(Cbx): suppressor of Contrabithorax location: 1-30. origin: Spontaneous. discoverer: E. B. Lewis. references: 1955, Am. Naturalist 89: 73-89. phenotype: Almost completely suppressed Cbx; wings made virtu- ally normal and segmental transformations strongly reduced. Without effect on the incidence of ether-induced bx pheno- copies (Capdevila and Garcia-Bellido, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 339-50). RK2. cytology: Placed in 7F1-8C6 based on its inclusion in Df(1)KA14 (Lefevre). # Su(crc): Suppressor of cryptocephal (J.C. Sparrow) location: 2-54.7. origin: Induced by ethyl methanesulfonate in l(2)crc cn chromo- some. discoverer: Sparrow, 1977. references: Sparrow, J.C., 1981, Genet. Res. 38: 297-314. phenotype: A dominant suppressor of l(2)crc lethality. Expres- sion is temperature sensitive in Su(crc) l(2)crc/l(2)crc heterozygotes and Su(crc) l(2)crc hemizygotes with a temperature-sensitive period beginning before pupariation and ending at the time of pupation. The effective lethal period for the suppressor genotypes at 30C is at the end of the pupal period, not during prepupal stages as is the case for l(2)crc homozygotes. cytology: Located between 38A7-B1 and 39C2-D1 but separable by deficiency mapping from l(2)crc which has been localized to 39C2-D1 and therefore Su(crc) is not a revertant of l(2)crc. # su(Cy) location: 3- not mapped. origin: Natural population. phenotype: Homozygotes without discernable phenotype except in the presence of Cy, in which case the curly-wing phenotype is suppressed. alleles: Two independent isolations of chromosomes with this effect (Meyer and Temin, 1965, DIS 40: 62 and Kosuda, 1971, Jpn. J. Genet. 46: 41-52). # Su(Cy): Suppressor of Curly location: 2- (not located). origin: Spontaneous in In(2LR)bwV1. discoverer: Thompson, 61e. references: 1963, DIS 38: 28. phenotype: Su(Cy)/Cy has wild-type wings. RK3. other information: Separable from In(2LR)bwV1. # Su(da): see SxlMI #*su(dx): suppressor of deltex location: 1-5. discoverer: Bridges, 35c26. synonym: suX-dx: suppressor in X chromosome of deltex. phenotype: Reduces phenotype of and imparts male fertility to dxst. RK2. # su(dpov): suppressor of dumpy-oblique vortex (T. Kjaer) location: 1- (proximal half of chromosome). references: Kjaer, 1986, DIS 63: 162. phenotype: Suppresses phenotype of dpov1 to normal or nearly normal; also suppresses dpov-DG37 and dpcm2 but does not suppress dpv2 or dpolv. Viability and fertility good. alleles: Three non-complementing, ethyl-methanesulfonate- induced alleles. allele synonym comments ___________________________________________________________ su(dpov)1 su(dpov)TK8-84 suppresses oblique and vortex su(dpov)2 su(dpov)TK25-84 suppresses oblique only su(dpov)3 su(dpov)TK26-84 suppresses oblique only #*Su(dx): Suppressor of deltex location: 2- (not located). origin: Spontaneous. discoverer: Bridges, 31a3. references: Morgan, Bridges, and Schultz, 1931, Year Book - Carnegie Inst. Washington 30: 410. phenotype: Su(dx)/+ reduces dxst to a slight but recognizable, fully fertile phenotype. Su(dx)/Su(dx) converts dxst to nearly wild type. RK3. # Su(dx)2 origin: Spontaneous. discoverer: Bridges, 31f1. references: Morgan, Bridges, and Schultz, 1931, Year Book - Carnegie Inst. Washington 30: 410. phenotype: Less effective than Su(dx) as a suppressor of dx. RK3. other information: Found in dx stock, as was Su(dx), along with ed. Su(dx)2 may simply be ed Su(dx) or it may be of indepen- dent origin. Allelism inferred from phenotype alone. # Su(en)28: see Dp(2;3)Su-en # Su(er): Suppressor of erupt location: 2- (near cn). origin: Present in many stocks. discoverer: Glass, 1941. references: 1944, Genetics 29: 436-46. 1957, Science 126: 683-89. phenotype: Only effect is suppression of er. Semidominant. Exposure to 1000 r of X rays from shortly after fertilization [8 min, according to Glass (1957), but not until 6 hr, according to Hildreth, 1968, Proc. Nat. Acad. Sci. USA 58: 1924-29] to middle of second larval instar inhibits Su(er), and er is then manifested in about 98% of flies. Tryptophan fed to larvae has similar effect. Some related compounds have a lesser effect; kynurenine and indole acetic acid have little or no effect. RK3. # su(f): suppressor of forked location: 1-65.9 (adjacent to and to the left of bb). references: Schalet and Lefevre, 1974, Chromosoma 44: 183-202. Schalet and Lefevre, 1976, The Genetics and Biology of Droso- phila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902. phenotype: su(f) mutations are found with several levels of reduced expression, and some if not all mutant alleles are sensitive to temperature. The weakest exhibit no phenotype when raised at 25 other than modification of the expression of specific alleles at other loci; increasingly reduced expres- sion leads to a specific phenotype, which variably includes Minute-like bristles, rough eyes with some anterior indenta- tion, reduced or absent ocelli, missing ocellar and other head and thoracic bristles, irregular acrostichal rows, excessive melanization, especially on head, and some crippling of legs; also wings may be blistery, broader, with extra veins and may be held upward and outward (Grell, CP627; Schalet, 1968, DIS 44: 125). The most severely affected alleles are lethal, the lethal period becoming earlier with increasing severity. At least one instance of interallelic complementation has been reported by an allele which in surviving adults exhibits pale yellow thread-like chaetae. Viable alleles act as allele- specific but locus-nonspecific modifiers. The locus was recognized by the nearly wild-type bristle phenotype of f su(f); some bristles slightly shortened or twisted at tips. Autonomous in gynandromorphs. f alleles fall into two classes: suppressible (f1, f4, and f5) and insuppressible (f3 and f3N)(Green, 1959, Heredity 13: 303-15). Suppressible alleles are spontaneous and contain insertions of transposable sequences; such alleles are also frequently modified by muta- tions in other modifier genes. For example, among alleles with gypsy inserts, su(f) suppresses ctk, lz1, f1, f5, bx34e, but not y2, Hw1, sc1, or ct6; all are suppressed by su(Hw). In addition, su(f) enhances the spontaneous mutants wa (copia) and lz37, but not we, lz34, lzk, s1, or v1 (412); all of these are affected by one or more other suppressor genotypes (Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97). Does not suppress the effect of f on the phenotype of dvr, i.e. crumpled wings (Lee, 1974, Aust. J. Biol. Sci. 27: 305-7). alleles: Allele specific features are detailed at the end of the entry. allele origin discoverer synonym ref ( comments | _____________________________________________________________________________________________________________________________ su(f)1 X ray Whittinghill, 37g4 suW(f) 22, 25, 30, 31, 32 viable allele; restriction map normal su(f)2 DES Lifschytz l(1)3DES 13, 22, 25, 29 ~500 bp insert in -3.5 to -3.3 su(f)3 DES Lifschytz l(1)D13 13, 16, 22 restriction map normal su(f)4 EMS Lifschytz l(1)R-9-18 13, 16, 17, 23, 25, 26 pale-bristle allele; ts lethal; su(f)pb restriction map normal su(f)5 X ray Schalet su(f)X1 ~150 bp deletion at +2.2 to +4.3 su(f)6 X ray Lifschytz l(1)X2 12, 16, 22, 23 ~1 kb deletion at -0.3 to +1.3 su(f)7 X ray Schalet su(f)X3 restriction map normal su(f)8 EMS Wright su(f)ts67g 2, 3, 10, 27 ts lethal; restriction map normal su(f)9 EMS Voss su(f)v 28, 29 viable derivative of su(f)2 su(f)10 EMS Lifschytz l(1)M171 15 on y+Ymal+ su(f)11 EMS Lifschytz l(1)M168 15 on y+Ymal+; pale-bristle allele ? su(f)12 EMS Russell l(1)ts726 1, 4, 6, 7, 18, 19, 20 ts lethal su(f)13 EMS Jurgens l(1)madts 8, 9, 10 ts lethal; restriction map normal su(f)14 EMS Wilson su(f)ts76a 33 ts lethal; restriction map normal su(f)15 X ray Lefevre l(1)GA46 14 su(f)16 X ray Lefevre l(1)GA130 14 su(f)17 X ray Lefevre l(1)HA16 14 su(f)18 X ray Lefevre l(1)HC148 14 su(f)19 X ray Lefevre l(1)L26 14 8 kb deletion in -3.4 to +6.4 su(f)20 X ray Lefevre l(1)N125 14 su(f)22 EMS Lefevre l(1)VE738 11, 14 su(f)23 P su(f)hd37 5 viable allele su(f)24 EMS Rutledge su(f)br 21 viable allele su(f)25 spont Schalet su(f)S1 ~200 bp insert in 0 to +2.1 su(f)26 spont Schalet su(f)S2 16, 17, 24 4.7 kb Doc element insert at +3.1 l(1)19-158 su(f)27 P Simmons su(f)MS97 5 1.1 kb P element insert at +0.2 su(f)28 P Simmons su(f)MS252 5 1.1 kb P element insert at +0.1 ( 1 = Clark and Russell, 1977, Dev. Biol. 57: 160-73; 2 = Dudick, Wright, and Brothers, 1974, Genetics 76: 487- 510; 3 = Fekete and Lambertsson, 1980, Hereditas 93: 169- 76; 4 = Girton, 1981, Dev. Biol. 84: 164-72; 5 = Girton, Langner, and Cejka, 1986, Roux's Arch. Dev. Biol. 195: 334-37; 6 = Girton and Russell, 1980, Dev. Biol. 77: 1-21; 7 = Girton and Russell, 1981, Dev. Biol. 85: 55-64; 8 = Jurgens and Gateff, 1979, Wilhelm Roux's Arch. Dev. Biol. 186: 1-27; 9 = Klose, Gateff, Emmerich, and Beikirch, 1980, Wilhelm Roux's Arch. Dev. Biol. 189: 57-67; 10 = Lambertson, 1975, Mol. Gen. Genet. 139: 145-56; 11 = Lefevre, 1981, Genetics 99: 461-80; 12 = Lifschytz and Falk, 1968, Mut. Res. 6: 235-44; 13 = Lifschytz and Falk, 1969, Mut. Res. 8: 147-55; 14 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 15 = Lifschytz and Yakobovitz, 1978, Mol. Gen. Genet. 161: 275-84; 16 = Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31; 17 = Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-521; 18 = Postlethwait, 1978, Wilhelm Roux's Arch. Dev. Biol. 185: 37-57; 19 = Russell, 1974, Dev. Biol. 40: 24-39; 20 = Russell, Girton, and Morgan, 1977, Wilhelm Roux's Arch. Dev. Biol. 183: 41-59; 21 = Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97; 22 = Schalet, 1968, DIS 43: 125; 23 = Schalet, 1972, DIS 49: 37, 64; 24 = Schalet, 1986, Mut. Res. 163: 115-144; 25 = Schalet and Lefevre, 1973, Chromosoma 44: 183-202; 26 = Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ash- burner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902; 27 = Suzuki, Kaufman, and Falk, 1976, The Genetics and Biology of Droso- phila (Ashburner and Novitski, eds.). Academic Press, Lon- don, New York, San Francisco, Vol. 1b, pp. 207-63; 28 = Voss, 1971, DIS 46: 55; 29 = Voss and Falk, 1973, Mutat. Res. 20: 221-34; 30 = Whittinghill, 1937, DIS 8: 11, 13; 31 = Whittinghill, 1938, Genetics 23: 305; 32 = Whittinghill, 1942, DIS 16: 70; 33 = Wilson, 1980, J. Embryol. Exp. Morph. 55: 243. | Coordinates are from O'Hare; the origin is at a salI site close to the insertion of the P element used to clone the gene. Positive values are toward the centromere. cytology: Placed in 20E-F by Lefevre (Schalet and Lefevre, 1973, Chromosoma 44: 183-202); polytene chromosomes in this region are refractory to analysis; however, it is generally accepted that su(f) is the most proximally located euchromatic gene on the X chromosome. molecular biology: Region cloned by O'Hare by means of transpo- son tagging using the P-element insert in su(f)28. 50 kb (-32 kb to +19 kb) restriction mapped; coordinate 0 designated as salI site 1.1 kb to the left of the P insert; positive values are to the right, toward the centromere. The region comprises single-copy DNA interspersed with repeated sequences. Repeated DNA found from -32.0 to -29.4, from -23.4 to -19.9, from -10.2 to -7.8, from -7.4 to -6.6, from -5.0 to -2.0, and from +4.9 to +19.0. Three major RNAs identified by RNA blot- ting and cDNA analysis; they are transcribed from the interval -0.3 to +3.7; their sizes are 1.3 kb comprising 3 exons, and 2.6 kb and 2.9 kb, both containing the same eight exons, including the three from the smaller RNA; they predict two proteins. DNA lesions detected so far in su(f) mutations con- fined to the region from -5.0 to +5.0 kb (O'Hare). Transfor- mation with -2.2 to +4.3 kb rescues lethality of su(f)2, su(f)5, su(f)6, su(f)19, and su(f)26 at 25; also covers suppression of forked-bristle phenotype in f su(f)1 (Simonelig and O'Hare). # su(f)1 phenotype: Wild type in appearance with normal viability and fertility when raised at 25; however, both su(f) flies raised at 29-30 and su(f)/Df(1)su(f) flies raised at 25 display the Minute-like syndrome. The same phenotype is seen in combina- tions with su(f)2 and su(f)6 raised at 29. su(f)/Df(1)su(f) is lethal when raised at 29; viability also temperature sensi- tive in combination with su(f)3 and su(f)5 (Schalet and Lefevre, 1976). su(f) enhances wa; wa su(f) eyes nearly white at 25 and white at 18 but apricot in flies raised at 29; suppresses lz1 and enhances lz37 at all temperatures. Increases the accumulation of gypsy transcript, suggesting that the wild-type allele represses gypsy (Parkhurst and Corces, 1986, Mol. Cell. Biol. 6: 2271-74); protein binding to a negative regulatory sequence of gypsy is reduced in nuclear extracts from su(f) pupae compared with those from wild type, again suggesting gypsy repression by su(f)+ (Mazo, Mizrokhi, Karavanov, Sedkov, Krichevskaha, and Ilyn, 1989, EMBO J. 8: 903-11). # su(f)2 phenotype: Homozygotes lethal at the larval stage; homozygous germ-line clones don't survive; no effect on development of peripheral or central nervous systems (Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31). Survives and suppresses f in combination with su(f)1 at 25, and exhibits M-like syn- drome in flies raised at 18. wa displays dilute apricot pig- mentation in su(f)1/su(f)2 flies raised at 25 but white eyes when raised at 18 (Schalet and Lefevre, 1976). su(f)2 shown to be proximal to su(f)1 by recombination (Schalet). # su(f)3 references: Schalet, 1972, DIS 49: 36-37. phenotype: Homozygous lethal. Fails to complement lethality of either su(f)3 or su(f)5. In combination with su(f)1 shows the M-like syndrome at 25 and is lethal at 29. # su(f)4 references: Schalet, 1972, DIS 49: 36-37. phenotype: May be the only pale-bristle allele. One other allele of this type was found by Dale Grace as a sex-lined lethal (Schalet). Recovered originally as a sex-linked reces- sive lethal, but fully viable, though weak, and suppresses f when raised at 18. Survivors exhibit pale-yellow, thread-like bristles, darker pigmentation dorsoanteriorly on thorax, and curled or wrinkled wings. Lethality at late pupal stage; homozygous germ-line clones show no maternal effect; also, no zygotic effects on development of peripheral or central ner- vous systems (Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31). Interactions of su(f)4 with other su(f) alleles are as follows: su(f)1, same as su(f)1 homozygotes at all temperatures; su(f)2, complementation for viability and bristle color and slight complementation for suppression of f; su(f)3, lethal at the time of puparium formation at 25, fully viable with some chaetae of all individuals showing the pale- bristle phenotype and the texture of the wings appearing abnormal at 18; su(f)5, fully viable and normal at 18, vari- able viability with a broad streak of dark pigment on thorax, which sometimes is concentrated at dorsal anterior region, and wings which may extend upward and outward at 25, lethal prior to puparium formation at 29; su(f)6, fully viable and normal at 18 and 25 but exhibiting the M-like syndrome at 29; Df(1)su(f), lethal at the time of puparium formation at 25 and just prior to eclosion at 18. Enhances wa; wa su(f) eyes white in flies raised at 25 and dilute apricot at 18; also enhances lz37 at 18. # su(f)6 phenotype: Homozygotes lethal at the larval stage; homozygous germ-line clones don't survive; no effect on development of peripheral or central nervous systems (Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31). Lethal with su(f)3 at 25 and with su(f)4 at 29. In combination with su(f)1, displays the M-like syndrome at 25 and lethal at 29. # su(f)8 references: Dudick, Wright, and Brothers, 1974, Genetics 76: 487-510. phenotype: The first allele recovered specifically as a temperature-sensitive lethal; completely lethal at 29; suppresses f at 25 but not at 18. Temperature-sensitive period for lethality from 50 to 140 h after oviposition, for f suppression coincident with bristle differentiation. Shift up to 30 before end of the second instar causes failure to pupariate; full-sized third instar larvae produced, which live 10-14 days; salivary-gland-secretion proteins specifically reduced or absent in these larvae, although the associated chromosome puffs appear normally; other proteins unaffected (Hansson, Lineruth, and Lambertsson, 1982, Wilhelm Roux's Arch. Dev. Biol. 190: 308-12); shift up prior to 70 h leads to little or no accumulation of Sgs transcripts as detected in Northern blots probed with sequences from Sgs3, Sgs4, Sgs7, and Sgs8, whereas a 48-h pulse beginning at 75 h is without effect on transcription or translation of Sgs genes (Hansson and Lambertsson, 1983, Mol. Gen. Genet. 192: 395-40). Shift up to 30 in early third instar blocks the increase in ecdys- terone titer normally occurring at the end of L3; ecdysterone supplementation induces abortive pupariation and stimulates prepupal polypeptide synthesis (Hansson and Lambertsson, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 48-51); leg discs of such larvae unable to evert, either in vivo or in vitro (Fek- ete and Lambertsson, 1980, Hereditas 93: 169-76). Homozygous females raised under permissive conditions, when shifted up to 30 cease laying eggs and the ovarian oocytes degenerate; fer- tility recoverable after pulses of three but not eleven hours (Dudick et al.). Heterozygotes with Df(1)su(f) at 25, su(f)1 at 29, and su(f)3 at 30 exhibit the M-like syndrome. Enhances M(3)67C, as indicated by reduced viability of su(f)8 versus su(f)+ sibs that are M(3)67C/+ (Girton, Langner, and Cejka, 1986, Roux's Arch. Dev. Biol. 195: 334-37). Enhances gypsy expression, more at 25 than at 18 (Parkhurst and Corces, 1986, Mol. Cell. Biol. 6: 2271-74). # su(f)9 references: Voss and Falk, 1973, Mutat. Res. 20: 221-34. phenotype: Recovered as a surviving son of su(f)3; still suppresses f, but is no longer lethal. X/Y males survive and have small rough eyes, broad outstretched wings and irregular abdominal pigmentation; homozygous females usually lethal with escapers showing the same phenotype as the males. XXY females survive and resemble XY males. X0 males die. su(f)9/su(f)3 never survives. Attributed by authors to a recessive variegated-position-effect suppressor of the lethality of su(f)3; locates to proximal extremity of the X; complements bb. cytology: Salivary chromosomes normal; pseudolinkage not tested. # su(f)12 references: Russell, 1974, Dev. Biol. 40: 24-39. phenotype: Selected as a cell-autonomous, temperature-sensitive lethal. Relative survival is 85% at 22, 75% at 25 and 1% at 29; temperature-sensitive period from first larval instar to early pupa. Homozygous females become sterile after two days at 29, whereas males so treated remain fertile. 23% of eggs laid at 29 fail to hatch; surviving larvae grow at subnormal rate and survive for up to twelve days, reaching the third instar; imaginal discs reduced greatly in size. 48-h pulses of 30 during late second and third instars results in consid- erable cell death in imaginal discs with a consequent deletion of some pattern elements and duplications of others in the head and legs; head duplications occur only in association with deficiencies; leg duplications seen as simply and com- plexly branched appendages involving variable numbers of joints. Pulses applied to early pupae lead to failure of his- toblast differentiation and applied later to the lack of chae- tae (Russell, Girton, and Morgan, 1977, Wilhelm Roux's Arch. Dev. Biol. 183: 41-59). Extensive use made of leg duplica- tions induced in su(f)12 in investigations of pattern forma- tion (Tiong, Girton, Hayes, and Russell, 1977, Nature 268: 435-37; Postlethwait, 1978, Wilhelm Roux's Arch. Dev. Biol. 185: 37-57; Girton and Russell, 1980, Dev. Biol. 77: 1-21; Girton, 1981, Dev. Biol. 84: 164-72; Girton and Russell, 1981, Dev. Biol. 85: 55-64). Enhances M(3)67C, as indicated by reduced viability of su(f)12 versus su(f)+ sibs that are M(3)67C/+ (Girton, Langner, and Cejka, 1986, Roux's Arch. Dev. Biol. 195: 334-37). # su(f)13 references: Jurgens and Gateff, 1979, Wilhelm Roux's Arch. Dev. Biol. 186: 1-25. phenotype: A cell-autonomous, temperature-sensitive recessive allele. Phenotype similar to that of su(f)12 except that trypan-blue staining provides no evidence of cell death resulting from heat shock at stages of development in which such treatment induces leg duplications. Authors postulate that su(f)12 discs developmentally impaired by heat shock, giving rise to observed abnormalities. Temperature-sensitive period from late second instar until two hours into puparia- tion. Shifts from 22 to 29 during the first larval instar leads to inability to pupariate; shifts between 112 and 164 h arrests adult development; shifts within the first six hours after the temperature for lethality removes bristles from the tergites. Gynandromorphs and somatic clones formed normally at permissive temperatures, but are not observed in adults produced at 29. Ecdysteroid level of larvae raised at 29 are less than one-tenth that of wild type; pupariation can be induced by ecdysterone supplementation (Klose, Gateff, Emmer- ich, and Beikirch, 1980, Wilhelm Roux's Arch. Dev. Biol. 189: 57-67). # su(f)14 references: Wilson, 1980, J. Embryol. Exp. Morphol. 55: 247- 56. phenotype: Temperature-sensitive lethal allele. Temperature- sensitive period for lethality extends from the second larval instar until twelve hours after pupariation. Shifting adult females to restrictive conditions results in the gradual abol- ition of oviposition; during the first day normal appearing eggs, many of which hatch, are produced, on the second day the hatchability of the eggs is reduced, and by day four the eggs are small and misshapen and lack chorions; oviposition ceases on the fifth or sixth day after shift up; at this time the ovary is deficient in stage 8-11 oocytes and lacks follicle cells indicating a breakdown in vitellogenesis. Shift back down to 25 leads to resumption of egg laying after four days. Ovarian response is autonomous in ovarian transplants. Fer- tility of males irreversibly impaired by shift up to 29. # su(f)23 references: Girton, Langner, and Cejka, 1986, Roux's Arch. Dev. Biol. 195: 334-37. phenotype: Homozygotes and hemizygotes survive at all tempera- tures from 18 to 29; complements the lethality of lethal alleles. The suppression of f is temperature sensitive, but the sensitivity is of opposite sign from that of other temperature-sensitive alleles; f su(f)23 flies raised at 18 have suppressed forked bristles, whereas those raised at 29 are forked; the temperature-sensitive period sharply confined to the short interval at which bristle development is ini- tiated. Does not appear to enhance M(3)67C. # su(f)24 phenotype: Similar to su(f)1; enhancement of wa, however, seen only in su(f)1/su(f)24. Closely linked to or inseparable from a variable recessive abnormality giving small misshapen eyes. #*Su(f): Suppressor of forked location: 2-74. origin: X ray induced. discoverer: Dobzhansky, 1931. synonym: SuD-f: Suppressor of forked of Dobzhansky. phenotype: Heterozygous Su(f) reduces expression of f; bristles blunt and wavy. Female fertility low. Homozygous lethal. RK3(A). other information: Crossing over probably reduced. # su(faswb): suppressor of facet-strawberry location: 1-1.96 (0.46 cm to the right of wa). origin: Spontaneous. references: Welshons and Welshons, 1986, Genetics 113: 337-54. phenotype: In the cis configuration with faswb it causes a facet-like rather than a glossy-like phenotype. Deficiencies for the element, when in cis with faswb, result in the com- plete suppression of faswb (Welshons and Welshons, 1985, Genetics 110: 465-77). Furthermore In(1)78b = In(1)3A2- 3;3C3-5 also suppresses faswb when in cis configuration. cytology: Placed in 3C2-5 based on its genetic position between wa and faswb and on the suppressive effect of In(1)78b. # Su(fu): Suppressor of fused location: 3 (not mapped). origin: Induced by ethyl methanesulfonate references: Busson, Limbourg-Bouchon, Mariol, Preat, and Lamour-Isnard, 1988, Roux's Arch. Dev. Biol. 197: 221-30. phenotype: Dominant suppressor of both the wing phenotype and the maternally determined lethality of fu mutants. other information: Four dominant partial suppressors observed in same experiment; not further characterized. # Su(Gl)27: Suppressor of Glued location: 1- {64}. origin: Induced by ethyl methanesulfonate. references: Harte and Kankel, 1982, Genetics 101: 477-501 (fig.). phenotype: Males carrying Su(Gl)27 in combination with Gl/+ are virtually wild type in phenotype, both with respect to the eye and to the optic lobe, when raised at 29; eye slightly reduced in size with some small facets scattered throughout the eye; facets not packed together as tightly as in wild type, some smooth pigmented material separating facets from one another. The optic lobe is very nearly normal in appearance; the lamina cell body region is thicker than in wild type and the lamina neuropil is slightly irregular in contour, but the medulla rotation and gross fiber tract abnormalities of Gl are miss- ing. Phenotype less nearly normal in flies raised at 18. Phenotypes of females not given; presumably recovered in heterozygous females and therefore dominant. Su(Gl)/Df(1)mal10 females exhibit outheld wings; probably not allelic to ot, which maps to the same region, since ot not included in Df(1)mal10. cytology: Placed in 19A5-E1 based on its inclusion in Df(1)mal10 = Df(1)19A5-6;19E1. # Su(Gl)57 location: 1- (not mapped). origin: Induced by ethyl methanesulfonate. references: Harte and Kankel, 1982, Genetics 101: 477-501. phenotype: Said to reduce the severity of Gl/+ at both 18 and 29, but genotypes not specified. # Su(Gl)77 location: 3- (between ru and h). origin: Induced by ethyl methanesulfonate. references: Harte and Kankel, 1982, Genetics 101: 477-501 (fig.). phenotype: Reduces the severity of Gl in flies raised at either 18 or 29. The most severe allele shows more normal facet arrays in the anterior than in the posterior part of the eye. The lamina cell body layer is thicker than normal in its pos- terior region and the lamina neuropil is somewhat misshapen, particularly anteriorly. The medulla is abnormally rotated, its posterior edge directly apposed to the lamina, but it is more normally organized than in Gl. The familiar abnormal projections from the posterior lamina through the medulla are present. The second optic chiasma is also divided into several tracts. In less extreme cases, the medulla is only slightly rotated and the second optic chiasma is normal. alleles: Although allelism not established, three independent mutations numbered 57, 102, and 160 with suppressing effects on Gl map between ru and h and are presumed to be allelic and are designated Su(Gl)771, Su(Gl)772, and Su(Gl)773, respec- tively. Of these Su(Gl)771 is the weakest Su(Gl)773 is inter- mediate and Su(Gl)772 is the strongest suppressor of Gl. # Su(H): Suppressor of Hairless location: 2-50.8. synonym: E(H); l(2)br7. references: Nash, 1965, Genet. Res. 6: 175-189. Nash, 1970, Genetics 64: 471-79. Ashburner, 1982, Genetics 101: 447-59. phenotype: Homozygous lethal; hemizygotes die in the pupal stage, between head eversion and the beginning of eye pigmen- tation. Heterozygotes in the absence of H are wild type in phenotype. Suppresses H; Su(H)/+; H/+ have 7-10 more bristles that H/+ alone; besides affecting the bristle phenotype of H, all alleles tend to enhance its wing-vein phenotype of shor- tening L4 and L5. Su(H) is without effect on the lethal phenotype of homozygous H. One homozygous-lethal allele acts as a dominant enhancer of H. Most alleles are amorphic or hypomorphic; heterozygous deficiencies for the locus also suppress, and duplications enhance H (Nash, 1970). Enhanced genotypes have 10-15 fewer bristles and a far more extreme loss of microchaetae on the thorax than their unenhanced coun- terparts. The number of bristles in H/+ flies is inversely related to the dose of Su(H)+, with the number of bristles varying from fewer than ten with four doses to approximately 35 with one dose. Some combinations of hypomorphic alleles produce occasional escapers; survivors have distinctive pheno- types, which are described under entries for specific alleles. alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________________ Su(H)1 spont Plunkett, 24i 1, 2, 3, 4 Su(H)2 spont Ashburner Su(H)AR9 1 Su(H)3 EMS Bodmer and Su(H)BMW4 1 hypomorphic Walker allele Su(H)4 EMS Bodmer and Su(H)BMW9 1 Walker Su(H)5 EMS Harrington Su(H)HG3 1 Su(H)6 EMS Harrington Su(H)HG36 1 Su(H)7 EMS Littlewood Su(H)LT3 1 Su(H)8 TEM Ashburner Su(H)SF8 1 Su(H)9 EMS O'Donnell Su(H)DM9 1 Su(H)10 EMS O'Donnell Su(H)DM15 1 Su(H)11 EMS O'Donnell Su(H)OK7 1 Su(H)12 P Shelton Su(H)MR1 1 Su(H)13 P Shelton Su(H)PI1 1 Su(H)14 P Shelton Su(H)PI3 1 Su(H)15 P Shelton Su(H)PI4 1 Su(H)16 EMS Littlewood Su(H)S5 1 hypermorphic allele ( 1 = Ashburner, 1982, Genetics 101: 447-59; 2 = Nash, 1965, Genet. Res. 6: 175-189; 3 = Nash, 1970, Genetics 64: 471- 79. 4 = Plunkett, 1926, J. Exp. Zool. 46: 181-244. cytology: Placed in 35B3-C1 on the basis of its inclusion in Df(2L)AR-R1 = Df(2L)35A3-4;35B9-C1 but not Df(2L)fn31 = Df(2L)34D3;35B3-5. # Su(H)3 phenotype: A leaky allele; trans heterozygotes with Su(H)1 show 20% survival; almost viable with Su(H)7; semilethal with Su(H)2, Su(H)4, Su(H)6, and Su(H)8; lethal in combination with Su(H)16. Survivors have vestigial wings and halteres and eyes somewhat reduced and rough; bristles normal. # Su(H)7 phenotype: Homozygous lethal; in trans heterozygotes with other alleles produces rare escapers, which have an extreme mutant phenotype; wings and halteres similar to those of an extreme vestigial allele; eyes, although large, have rough glazed appearance and the flies are almost achaetous, having fewer than ten macrochaetae per fly; acrostichal hairs and other microchaetae reduced in number and disturbed in arrangement; tarsal claws also much reduced. # Su(H)16 phenotype: Homozygous lethal; acts as a dominant enhancer of H, with about the same effect as heterozygosity for a duplication for the locus. # su(Hw): suppressor of Hairy wing location: 3-54.8. references: Lewis, 1949, DIS 23: 59-60. Klug, Bodenstein and King, 1968, J. Exp. Zool. 167: 151-56. Klug, King, and Wattiaux, 1970, J. Exp. Zool. 174: 125-40. Modolell, Bender, and Meselson, 1983, Proc. Nat. Acad. Sci. USA 80: 1678-82. Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97. phenotype: In homozygous condition (e.g., su(Hw)2/su(Hw)2 or su(Hw)2/su(Hw)7) suppresses certain spontaneous alleles that contain gypsy inserts at a number of different loci, e.g., y2, Hw1, sc1, scD2, dm1, ct6, ctK, lz1, f1, f5, fK, B, Bxd2, h1, bx3, bx34e, bxd, bxd51j, bxd55i, bxdK, and ci1; alleles without gypsy inserts are not suppressed (see Lewis, 1949). Apparent exceptions to the above generalizations are scD1, which is suppressed and reportedly X ray induced and rsP1 and rsP2, both of which show temperature-sensitive suppression but no evidence of gypsy insertion. With the exception of lz37, which is enhanced by su(Hw), alleles not known, or known not, to contain gypsy, but which are modified by other suppressors are unaffected by su(Hw). Two alleles, ctK and fK, exhibit suppression in heterozygotes for either su(Hw) or a deficiency for su(Hw). su(Hw) causes accumulation of f transcript in flies carrying f alleles that ordinarily display low levels to return to wild-type levels (Parkhurst and Corces, 1985, Cell 41: 429-37); judging from results with y2, this is caused by reduction of transcription from the associated gypsy element (Parkhurst and Corces, 1986, Mol. Cell. Biol. 6: 47-53). Females homozygous for su(Hw)1, su(Hw)2, su(Hw)3, and su(Hw)4 are sterile; females homozygous for su(Hw)8 and transheterozy- gotes of su(Hw)7 with other allelles are fertile; su(Hw)7/su(Hw)2 are fertile and, in fact, suppress the female sterility of dm and lz (Grell). In sterile combinations, vitellogenesis inhibited leading to smaller-than-normal cysts surrounded by multiple layers of follicle cells; nurse cell chromosomes remain condensed until stage 9, after which egg chambers degenerate; ovarian phenotype autonomous in tran- splants (Klug et al., 1968, 1970). Reduced viability attri- buted to some alleles apparently caused by extraneous genes, since those alleles are perfectly viable in combination with su(Hw) deficiencies. alleles: allele origin discoverer synonym ref ( comments ___________________________________________________________________ *su(Hw)1 spont Bridges, 23e4 1 su(Hw)2 spont Lewis, 1948 2, 3, 5 1.3 kb insert su(Hw)3 EMS Grell su(Hw)69k 3, 4, 5 Southern blot normal su(Hw)4 EMS Grell su(Hw)70a 3, 5 su(Hw)5 / ray Coyne su(Hw)B 4 Molecular de- letion su(Hw)6 / ray Coyne su(Hw)C 4 Molecular de- letion su(Hw)7 spont Grell su(Hw)f 3, 4 Southern blot normal; in TM6 su(Hw)8 spont Grell su(Hw)f3 3, 4 0.7 kb insert ( 1 = Bridges, 1932, Proc. Int. Congr. Genet. 6th, Vol. 2: 12-14; 2 = Lewis, 1949, DIS 23: 59-60; 3 = Modolell, Bender, and Meselson, 1983, Proc. Nat. Acad. Sci. USA 80: 1678-82; 4 = Parkhurst, Harrison, Remington, Spana, Kelley, Coyne, and Corces, 1988, Genes Dev. 2: 1205-15; 5 = Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97. cytology: Placed in 88A12-B5 based on its inclusion in Df(3R)red-P52 = Df(3R)88A12-B1;88B4-5 [Lewis, 1981, Develop- mental Biology Using Purified Genes (Brown and Fox, eds.). Academic Press, New York, pp. 189-208]. molecular biology: Region cloned and sequenced by Parkhurst, Harrison, Remington, Spana, Kelley, Coyne, and Corces (1988, Genes Dev. 2: 1205-15); normal allele produces a 3.3 kb mes- sage which is expressed throughout development, and is expressed in ovaries; transcription from right to left, i.e., from the tip of 3R toward the centromere. Genomic sequence comprises seven exons, separated by six introns, all but the first of which are short, in the range of 50-60 base pairs. Conceptual amino-acid sequence corresponds to a 109,000 dalton polypeptide; it contains twelve Zn finger motifs in the middle of the protein encoded by sequences contained in several of the miniexons and a highly acidic region (48% Asp + Glu) between amino acids 154 and 202 immediately preceding the first Zn finger; structure suggests a transcription factor. Nuclear extracts or partially purified protein from overex- pressing E. coli or Drosophila cells bind to a 367 base pair DNA sequence containing twelve copies of PyPuTTGCATACCPy from the 5' untranslated end of gypsy between the 5' LTR and the initial ATG (Spana, Harrison, and Corces, 1988, Genes Dev. 2: 1414-23; Mazo, Mizrokhi, Karavanov, Sedkov, Krichevskaja, and Ilyn, 1989, EMBO J. 8: 903-11); footprinting indicates protection of a 55 bp domain by su(Hw) protein. Antibodies raised against the protein label 100 to 200 sites on polytene chromosomes (Spana et al.). # su(lz34): suppressor of lozenge-34 location: 3- (not located). origin: Spontaneous. discoverer: H. A. Bender. references: Bender and Green, 1960, Genetics 45: 1563-66. phenotype: lz34; su(lz34) eyes larger, less rough, and more normal in color than lz34 alone. Female distinctly more fer- tile with su(lz34) but still lacks parovaria and spermathecae. RK2. # Su(M): Suppressor of Minute These are tandem duplications selected on the basis of their normal phenotype in heterozygous combination with a specific Minute. They are treated under Dp(2;2)M+ and Dp(3;3)M+. # su(msm1) location: 2- (not mapped). origin: Induced by ethyl methanesulfonate. references: Nishida, 1980, Jpn. J. Genet. 55: 427-39. phenotype: Most males homozygous for su(msm1) and ms(3)m1 have small spiral-shaped testes and motile sperm in their seminal vesicles, whereas those homozygous for ms(3)m1 have rudimen- tary testes. # Su(par): Suppressor of paralog location: 1- to the right of v. references: Thierry-Mieg, 1982, Genetics 100: 209-37. phenotype: Semidominant. In homozygous condition reduces the incidence of agametic par/par females from 95-100% to 51-61% and abdominal defects from 26-49% to 5-14%. No effect on fecundity at 29 or the frequency of cephalic defects caused by par. par+/par Su(par) females are 77% agametic. Su(par) homozygotes in the absence of par are normal. # Su(Pc)37D: Suppressor-of-Polycomb-37D location: 2-{54}. references: Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40. phenotype: Suppresses Pc. cytology: Located at 37D2 to 38C1. # su(pr): suppressor of purple location: 3-95.5. references: Schultz and Bridges, 1932, Am. Nat. 66: 323-34. Rutledge, Mortin, Kelley, and Meselson, 1988, Genetics 119: 391-97. phenotype: Completely suppresses pr1 but not v1 both of which contain an insert of transposable element 412, and both of which are suppressed by su(s). Also suppresses both lz34 and lzk; among alleles with gypsy inserts, su(pr) suppresses ctK, f1, and f5, enhances Hw1, ctK, bx3, and bx34e, but has no influence on the expression of y2, sc1, or ct6. No visible mutant phenotype. Abnormal phenotypes, low viability and sterility described for su(pr)1 and su(pr)B extraneous to su(pr), since su(pr)B/su(pr)1 displays normal viability and fertility. alleles: allele origin discoverer synonym ref ( comments _________________________________________________________________ *su(pr)1 spont Stern, 27C2 3, 4, 5 In(3R)su(pr) su(pr)2 spont Bridges, 29a13 su(pr)B 1, 2, 3 su(pr)3 EMS? Grell su(pr)e3 2 su(pr)4 EMS? Grell su(pr)e4 2 ( 1 = Bridges, 1932, Z. Indukt. Abstamm. Vererbungsl. 60: 207-18; 2 = Rutledge, Mortin, Kelley, and Meselson, 1988, Genetics 119: 391-97; 3 = Schultz and Bridges, 1934, Am. Nat. 66: 323-34; 4 = Stern, 1929, Z. Indukt. Abstamm. Vererbungsl. 52: 373-89; 5 = Stern, 1934, DIS 1: 35. # su(r): suppressor of rudimentary location: 1-27.7. references: Bahn, 1972, DIS 49: 38 & 98. Str/man, Bahn, N/rby, and Sick, 1973, Hereditas 73: 239-46 (fig.). Str/man, 1974, Hereditas 78: 157-68. phenotype: Suppresses both the phenotypic effects and the female sterility of all r alleles; also suppresses the r phenocopying and lethal effects of 6-azauracil administration. Little or no dihydrouracil dehydrogenase (EC 1.3.99.11) activity. Thought to interfere with pyrimidine catabolism. Unable to degrade uracil and extremely sensitive to exogenous pyrimidine. Enhances the expression of dp and net, and causes b flies to have very black bodies, darker than wild type, especially along the wing veins; forms synthetic lethals in combination with tt and whd. alleles: Ten ethyl-methanesulfonate-induced alleles recorded; one by Bahn and nine by Falk and DeBoer (1980, Mol. Gen. Genet. 180: 419-24). # su(s): suppressor of sable (R.A. Voelker) location: 1-0+ [rare crossovers occur between y and su(s)]. references: Bridges, 1919, Anat. Rec. 15: 357-58. Schultz and Bridges, 1932, Am. Nat. 66: 323-34. Shapard, 1960, Genetics 45: 359-76. Baglioni, 1960, Heredity 15: 87-96. Hayman and Maddern, 1972, DIS 49: 72. Maddern, R.M., 1973, Ph.D. Thesis, Univ. Adelaide, Australia. Jacobson, Grell, Yim and Gardner, 1982a, Genet. Res. 40: 19- 32. Jacobson, Yim, Grell and Wobbe, 1982b, Cell 30: 817-23. Chang, Wisely, Huang and Voelker, 1986, Mol. Cell. Biol. 6: 1520-28. Rutledge, Mortin, Schwarz, Thierry-Mieg and Meselson, 1988, Genetics 119: 391-97. Searles and Voelker, 1986, Proc. Nat. Acad. Sci. USA 83: 404-08. Voelker, Huang, Wisely, Sterling, Bainbridge and Hiraizumi, 1989, Genetics 122: 625-42. phenotype: In hemizygous or homozygous condition suppresses certain spontaneous alleles that contain 412 insertions at several loci (e.g., v, v2, vk, pr, prbw, sp) or hybrid dysgenesis-induced alleles that contain P element insertions (e.g., snw, y76d28). s is suppressible but does not have a 412 insertion (Searles and Voelker, 1986). bx is caused by a 412 insertion but is not suppressed (Voelker et al., 1989). Not all su(s) alleles suppress all suppressible alleles (Jacobson et al., 1982a). Although reported as recessive, some alleles show a slight dominance (Shapard, 1960; Baglioni, 1960). No lethal alleles recovered in a lethal saturation screen of the su(s) region, but a number of X-ray-, EMS- and ENU-induced alleles exhibit sterility or reduced male fertil- ity when reared at 18C (Voelker et al., 1989). Some alleles cause a slight spreading of the wings, especially in males. Suppression of v and y76d28 occurs by elevating the levels of pseudo-wild-type, presumably translatable, message (Searles, Ruth, Pret, Fridell, and Ali, submitted; P. Geyer, V. Corces and M. Green, personal communication). Some alleles enhance some gypsy-caused mutations (Rutledge et al., 1988). A dupli- cation of su(s)+ enhances suppressible pr alleles (Jacobson et al., 1982b). alleles: allele origin discoverer synonym ref comments _____________________________________________________________________________________________________________________________________ *su(s)1 spont Bridges 1 su(s)2 spont Bridges 1, 2, 4 gypsy insertion in first intron associated with 425 bp deletion; gypsy excised leaving solo LTR in su(s)2 wa cv t stock su(s)3 X ray Schultz 1, 2, 12 No abnormality on Southern; enhances some gypsy-caused mutations su(s)4 spont Stern suS2-v pr 1, 2, 4, 10 rambler insertion in first intron su(s)S *su(s)5 X ray Green su5016-v 1 su(s)501 su(s)6 spont Shapard su(s)51c15 1, 2, 4, 6 gypsy insertion in first intron su(s)7 spont Green su51j6-v 1, 2, 4 gypsy insertion in first intron su(s)51j *su(s)8 spont Green su52c-v 1 su(s)52c su(s)9 spont Maddern su(s)68i 2, 4, 5 weak, variable suppressor, good viability; su(s)1270 rover insertion in first intron *su(s)10 EMS Maddern su(s)68h 5 strong suppressor, reduced viability *su(s)11 NNG Maddern su(s)68j10 5 very strong suppressor, very low viability *su(s)12 EMS Maddern su(s)68j21 5 very strong suppressor, low viability *su(s)13 EMS Maddern su(s)68j23 5 weak, variable suppressor, good viability *su(s)14 EMS Maddern su(s)68j25 5 medium suppressor, low viability *su(s)15 EMS Maddern su(s)681(1) 5 strong suppressor, low viability *su(s)16 EMS Maddern su(s)681(2) 5 strong suppressor, low viability *su(s)17 EMS Maddern su(s)681(3) 5 strong suppressor, very low viability *su(s)18 EMS Maddern su(s)69f11 5 weak, variable suppressor *su(s)19 EMS Maddern su(s)69f14 5 very strong suppressor *su(s)20 EMS Maddern su(s)69f19 5 strong suppressor *su(s)21 X ray Maddern su(s)69g7 5 strong suppressor, good viability *su(s)22 X ray Maddern su(s)69g11 5 strong suppressor, good viability *su(s)23 X ray Maddern su(s)69g12 5 strong suppressor, good viability *su(s)24 X ray Maddern su(s)691(1) 5 weak suppressor, reduced viability *su(s)25 X ray Maddern su(s)691(2) 5 strong suppressor, good viability *su(s)26 X ray Maddern su(s)691(3) 5 strong suppressor, good viability *su(s)27 X ray Maddern su(s)691(4) 5 weak, variable suppressor, good viability su(s)28 DNA trans- Fox su(s)e5.6 8, 10 Delta 88 insertion in first intron; does formation not suppress sp su(s)29 DNA trans- Germeraad su(s)66 9 17.6 insertion in first intron formation su(s)30 EMS Grigliatti su(s)J1 7 normal Southern su(s)31 EMS Grigliatti su(s)J8 7 normal Southern su(s)32 EMS Grigliatti su(s)J18 7 normal Southern su(s)33 EMS Grigliatti su(s)J24 7 normal Southern su(s)34 EMS Grigliatti su(s)J30 7 normal Southern su(s)35 X ray Grell su(s)X1 10 normal Southern, cs male fertility su(s)36 X ray Grell su(s)X4 10 normal Southern su(s)37 EMS Grell su(s)e1 10 normal Southern, cs male fertility su(s)38 EMS Grell su(s)e6 10 normal Southern, poor viability su(s)39 HD Voelker su(s)W20 2, 4 P element insertion in untranslated leader su(s)40 spont Carpenter su(s)ab 2, 4, 10 HMS Beagle insertion in first intron; does not suppress sp su(s)41 spont Voelker su(s)83f1 2, 4 roamer insertion in first intron su(s)42 HD Green su(s)83f24(8) 2, 4 P element insertion in untranslated leader, induced in R(1)2 su(s)43 HD Green su(s)83f24(10) 2, 4 P element insertion in first intron, induced in R(1)2 su(s)44 HD Green su(s)83g2(15) 2, 4 P element insertion in untranslated leader, induced in R(1)2 su(s)45 HD Green su(s)83g2(22) 2, 4 P element insertion in untranslated leader, induced in R(1)2 su(s)46 HD Green su(s)83g2(10) 13 induced in R(1)2 su(s)47 spont Voelker su(s)84a 4 springer insertion in first intron su(s)48 ENU Voelker su(s)A17 3 normal Southern su(s)49 ENU Voelker su(s)A18 3 normal Southern, cs male fertility su(s)50 ENU Voelker su(s)A65 3 normal Southern su(s)51 ENU(spont?) Voelker su(s)A66 3, 4 roamer insertion in first intron su(s)52 ENU Voelker su(s)A67 3 normal Southern, cs male fertility su(s)53 ENU Voelker su(s)A68 3 normal Southern su(s)54 ENU Voelker su(s)A107 3 normal Southern, cs male fertility su(s)55 ENU Voelker su(s)B2 3 normal Southern, induced in Dp(1;3)E1 su(s)56 ENU Voelker su(s)B6 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 su(s)57 ENU Voelker su(s)B7 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 *su(s)58 ENU Voelker su(s)B8 3 induced in Dp(1;3)E1 su(s)59 ENU Voelker su(s)B13 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 su(s)60 ENU Voelker su(s)B14 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 su(s)61 ENU Voelker su(s)B15 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 su(s)62 ENU Voelker su(s)B16 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 su(s)63 ENU Voelker su(s)B17 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 su(s)64 ENU Voelker su(s)B18 3 normal Southern, induced in Dp(1;3)E1 su(s)65 ENU Voelker su(s)B22 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 *su(s)66 ENU Voelker su(s)B25 3 induced in Dp(1;3)E1 su(s)67 ENU Voelker su(s)B26 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 su(s)68* ENU Voelker su(s)B27 3 induced in Dp(1;3)E1 su(s)69 EMS Voelker su(s)C1 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 su(s)70 EMS Voelker su(s)C2 3 normal Southern, cs male fertility, induced in Dp(1;3)E1 su(s)71 spont Simmons su(s)sn-w 11 unidentified insertion; suppresses some P element-caused sn alleles su(s)72 EMS Rutledge su(s)44 12 enhances some gypsy-caused mutations su(s)73 / ray Voelker su(s)87k1 13 induced in Dp(1;3)E1 su(s)74 / ray Voelker su(s)88a1 13 induced in Dp(1;3)E1 su(s)75 / ray Voelker su(s)88a2 13 induced in Dp(1;3)E1 su(s)76 / ray Voelker su(s)88a3 13 induced in Dp(1;3)E1 su(s)77 / ray K. White su(s)g1 14 su(s)78 / ray K. White su(s)g2 14 su(s)79 / ray K. White su(s)g3 14 su(s)80 / ray K. White su(s)g4 14 su(s)81 / ray Voelker su(s)89a1 13 induced in Dp(1;3)E1 su(s)82 / ray Voelker su(s)89a2 13 induced in Dp(1;3)E1 su(s)83 / ray Voelker su(s)89a3 13 induced in Dp(1;3)E1 su(s)84 / ray Voelker su(s)89a4 13 induced in Dp(1;3)E1 su(s)85 / ray Voelker su(s)89a5 13 induced in Dp(1;3)E1 su(s)86 / ray Voelker su(s)89a6 13 induced in Dp(1;3)E1 su(s)87 / ray Voelker su(s)89b1 13 induced in Dp(1;3)E1 su(s)88 / ray Voelker su(s)89b2 13 induced in Dp(1;3)E1 su(s)89 / ray Voelker su(s)89b3 13 induced in Dp(1;3)E1 su(s)90 / ray Voelker su(s)89b4 13 induced in Dp(1;3)E1 su(s)91 / ray Voelker su(s)89b5 13 induced in Dp(1;3)E1 su(s)92 / ray Voelker su(s)89b6 13 induced in Dp(1;3)E1 su(s)93 / ray Voelker su(s)89b7 13 induced in Dp(1;3)E1 su(s)94 HD Green su(s)89g1 15 P element insertion; suppresses y76d28 *su(s)95 HD Green su(s)89g2 15 P element insertion; suppresses y76d28 su(s)96 / ray Voelker su(s)f2 13 su(s)97 / ray Voelker su(s)f3 13 su(s)98 / ray Voelker su(s)f4 13 su(s)99 / ray Voelker su(s)f15 13 su(s)100 / ray Voelker su(s)f25 13 su(s)101 / ray Voelker su(s)f35 13 su(s)102 / ray Voelker su(s)f39 13 su(s)103 / ray Voelker su(s)f42 13 su(s)104 / ray Voelker su(s)f43 13 su(s)105 / ray Voelker su(s)f49 13 su(s)106 / ray Voelker su(s)f54 13 su(s)107 / ray Voelker su(s)f57 13 su(s)108 / ray Voelker su(s)f59 13 su(s)109 / ray Voelker su(s)f61 13 su(s)110 / ray Voelker su(s)f66 13 su(s)111 / ray Voelker su(s)f67 13 su(s)112 / ray Voelker su(s)f68 13 su(s)113 / ray Voelker su(s)f71 13 su(s)114 / ray Voelker su(s)f72 13 su(s)115 / ray Voelker su(s)f76 13 su(s)116 / ray Voelker su(s)f77 13 su(s)117 / ray Voelker su(s)f80 13 su(s)118 / ray Voelker su(s)f83 13 su(s)119 / ray Voelker su(s)f85 13 su(s)120 / ray Voelker su(s)m5 13 induced in Dp(1;Y)y+ sc su(s)121 / ray Voelker su(s)m18 13 induced in Dp(1;Y)y+ sc su(s)122 / ray Voelker su(s)m27 13 induced in Dp(1;Y)y+ sc su(s)123 / ray Voelker su(s)m44 13 induced in Dp(1;Y)y+ sc su(s)124 / ray Voelker su(s)m48 13 induced in Dp(1;Y)y+ sc su(s)125 / ray Voelker su(s)m72 13 induced in Dp(1;Y)y+ sc su(s)126 / ray Voelker su(s)m77 13 induced in Dp(1;Y)y+ sc su(s)127 / ray Voelker su(s)m78 13 induced in Dp(1;Y)y+ sc su(s)128 / ray Voelker su(s)m80 13 induced in Dp(1;Y)y+ sc su(s)129 / ray Voelker su(s)m90 13 induced in Dp(1;Y)y+ sc su(s)130 / ray Voelker su(s)m94 13 induced in Dp(1;Y)y+ sc su(s)131 / ray Voelker su(s)m100 13 induced in Dp(1;Y)y+ sc su(s)132 / ray Voelker su(s)m103 13 induced in Dp(1;Y)y+ sc su(s)133 / ray Voelker su(s)m105 13 induced in Dp(1;Y)y+ sc ( 1 = CP627; 2 = Chang, Wisely, Huang and Voelker, 1986, Mol. Cell. Biol. 6: 1520-28; 3 = Voelker, Huang, Wisely, Ster- ling, Bainbridge and Hiraizumi, 1989, Genetics 122: 625-42; 4 = Voelker, Graves, Gibson and Eisenberg (in preparation for Genetics); 5 = Maddern, 1973, Ph.D. Thesis, Department of Genetics, University of Adelaide; 6 = Shapard, 1960, Genetics 45: 359-76; 7 = Grigliatti, personal communica- tion; 8 = Fox, 1977, Molecular Genetic Modification of Eukaryotes, (Rubenstein et al., eds.). pp. 101-31; Fox and Yoon, 1970, Proc. Nat. Acad. Sci. USA 67: 1608-15; 9 = Ger- meraad, 1975, Genetics 80: 534-35; 1976, Nature 262: 229- 31; 10 = Jacobson, Grell, Yim and Gardner, 1982, Genet. Res. 40: 19-32; 11 = Simmons, unpublished data; 12 = Rutledge, Mortin, Schwarz, Thierry-Mieg and Meselson, 1988, Genetics 119: 391-97; 13 = Voelker, unpublished data; 14 = White, unpublished data; 15 = Green, unpublished data. cytology: Placed in 1B10-1C1 (Hayman and Maddern, 1972; Chang et al., 1986). molecular biology: An 8 kb region that rescues su(s) mutations when reintroduced by P element-mediated transformation of embryos was sequenced (R. Voelker, W. Gibson, J. Graves, J. Sterling and M. Eisenberg, in preparation). A 7.8 kb primary transcript that is produced throughout the life cycle is tran- scribed telomere to centromere. It is processed to a ~5 kb mature message by splicing out five introns that range in size from 60 to 2053 nucleotides, the latter occurring within but near the 3' end of a ~500 nucleotide nontranslated leader. All eleven spontaneous mutations examined contain mobile ele- ment insertions within the 2053 nt intron. One dysgenesis- induced allele contains a P element insertion within that same intron, whereas four other alleles contain P element inser- tions within the nontranslated leader 5' to the large intron (R. Voelker, J. Graves, W. Gibson and M. Eisenberg, in preparation). The conceptual protein is a ~145,000 dalton polypeptide that contains an opa-like sequence and a highly charged region similar to regions of some RNA-binding/splicing proteins. The protein is located primarily in the nucleus. # Su(S): Suppressor of Star location: 2-3; based on cytological location between shr (2- 2.3) and dpp (2-4.0). origin: Synthetic. discoverer: Curry, 37b. references: Morgan, Bridges, and Schultz, 1937, Year Book - Carnegie Inst. Washington 36: 301. Lewis, 1945, Genetics 30: 154. phenotype: Su(S)/S and Su(S)/+ wild type. RK2A. cytology: Associated with the deficiency for 22D1 to 22E1 or the deficiency for 33F to 34A9, or both, derived by combining the left end of In(2L)Cy = In(2L)22D1-2;33F5-34A1 and the right end of In(2L)t = In(2L)22D3-E1;34A8-9. According to Lewis (1945), the region between 22D1 and 22E1 is more likely responsible. #*Su(sc): Suppressor of scute location: 3-59. discoverer: Payne. synonym: sc-Inh-3: scute Inhibitor on chromosome 3; Ext-sct-3. references: 1921, Genetics 5: 501-42. Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 158. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 225, 235. phenotype: Tends to restore bristles removed by sc in Su(sc)/+ heterozygotes. RK3. # su(SD): suppressor of Segregation Distortion location: 1-49.5 [53/74 of the distance from g to sd (Waddle, Owens, and Petty)]. references: Sandler, 1962, Am. Nat. 96: 161-65. Sandler and Rosenfeld, 1962, Can. J. Genet. Cytol. 4: 453-57. Katakoa, 1967, Jpn. J. Genet. 42: 327-33. Waddle and Oster, 1977, DIS 52: 5. phenotype: Several X chromosomes that reduce the k value in SD/+ males from nearly 1.0 to a value closer to 0.5. Not clear that the various X-linked suppressors of distortion are related. # Su(sph): Suppressor of sparse hairs location: 2-24 or 25. synonym: Su-x4. references: Voss and Falk, 1973, Mutat. Res. 20: 221-34. phenotype: Allele specific suppressor of sph. Su(sph) permits survival of sph4 but not sph7 males; both homozygous and heterozygous Su(sph) allow 50 to 60% control survival. sph4 females are rescued by homozygous but not heterozygous Su(sph) to nearly 20% of control. alleles: One spontaneous allele [Su(sph)1] and one induced by X rays [Su(sph)2]. cytology: Polytene chromosomes normal. #*Su(ss): Suppressor of spineless location: 3-61 (between bx and sr). origin: Spontaneous. discoverer: Bridges, 22g15. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 236. phenotype: Su(ss)/+ converts ss/ss to wild type except for reduced and erect posterior scutellars. Homozygous lethal. RK2. # Su(ss)2 origin: Spontaneous. discoverer: E. B. Lewis, 1947. references: 1950, DIS 24: 59. phenotype: Homozygous or heterozygous Su(ss)2 causes ss to have long bristles that are only slightly thin, like a mild Minute; however, the posterior scutellars remain greatly reduced as in unsuppressed ss. Temperature-sensitive allele; suppression more extreme at 29 than at 17; temperature-sensitive period from 5-34 h after onset of puparium formation (Mglinetz, Ivanov, and Kostina, 1978, Ontogenez 9: 136-41). RK2. # Su(ss)3 origin: Spontaneous. discoverer: Hexter, 1950. references: 1953, DIS 27: 55-56. phenotype: ss Su(ss)3 homozygote wild type for all bristles; ss Su(ss)3/ss + intermediate between ss and wild type. ss Su(ss)3/ss bx Su(ss)2 is wild type. RK2. # Su(Ste): Suppressor of Stellate location: Y-between kl2 and kl1. references: Meyer, Hess, and Beerman, 1961, Chromosoma 12: 676-716. Hardy and Kennison, 1980, DIS 55: 55. Gatti, M. and S. Pimpinelli, 1983, Chromosoma 88: 349-373. Hardy, Lindsley, Livak, Lewis, Sivertsen, Joslyn, Edwards, and Bonaccorsi, 1984, Genetics 107: 591-610. Livak, 1984, Genetics 107: 611-634. Livak, 1990, Genetics 124: 303-16. phenotype: Designates the region of the Y chromosome whose presence decreases both abundance and splicing of the X-linked Ste transcripts. Ste males deficient for Su(Ste) display abundant star-shaped aggregates of needle-shaped crystals in the nuclei and cytoplasm of their primary spermatocytes; their spermatids contain micronuclei and nebenkerne of nonuniform size; and they are sterile. Ste+ males deficient for Su(Ste) have one or more long needle-shaped crystals in their primary spermatocytes and micronuclei and irregular nebenkerne in their spermatids; these males are fertile and display irregu- lar disjunction as follows: (1) both the sex chromosomes and the large autosomes undergo nondisjunction, (2) the fourth chromosomes disjoin regularly, (3) sex chromosome nondisjunc- tion is more frequent in cells in which the second or third chromosomes nondisjoin than in cells in which autosomal dis- junction is regular, (4) in doubly exceptional cells, the sex chromosomes tend to segregate to the opposite pole from the autosomes, and (5) there is meiotic drive; i.e., reciprocal meiotic products are not recovered with equal frequencies, complements with fewer chromosomes being recovered more fre- quently than those with more chromosomes. Two smaller com- ponent deficiencies of the Su(Ste) deficiency display a normal meiotic phenotype in Ste+ males and low levels of meiotic non- disjunction in Ste males. cytology: Placed primarily in the Hoechst-dull region h11 of the Y chromosome, between the Y breakpoints of T(1;Y)P7 = T(1;Y)h33;h11 and T(1;Y)E15 = T(1;Y)h26-29;h12-13. molecular biology: Comprises approximately 80 copies of a sequence that is partly homologous to the Ste sequences on the X chromosome; actually the number of repeats varies over a three-fold range in Y's from natural populations (Lyckegaard and Clark, 1989, Proc. Nat. Acad. Sci. USA 86: 1944-48). The repeat length, however, is 2.6-2.8 kb compared to 1.15-1.25 for Ste. The majority of these sequences lie proximal to the breakpoint of T(1;Y)P7 = T(1;Y)h33;h11; and distal to that of T(1;Y)E1 = T(1;Y)h26;h11; all Su(Ste) sequences lie distal to the breakpoint of T(1;Y)E15 = T(1;Y)h26-29;h12-13. Deletions for most or all of these sequences results in abundant spliced Ste RNA in the testes, compared the less abundant and largely unspliced transcripts detectable in XY males. Results from partial deletions more nearly resemble those from XY than from X0 testes. Sequences of two Su(Ste) repeats show segments homologous to Ste and totally unrelated segments; the homolo- gous regions show a number of single nucleotide substitutions, including one that alters a splice-acceptor site; the sequence also contains an insert of a variable number of AAC repeats. # Su(stn): Suppressor of stoned location: 1-22 (between sn and oc). references: Kelly, Hannan, and Petrovich, 1987, J. Neurogenet. 4: 144-45. phenotype: Suppresses both the behavioral and the viability effects of stn. # su(t): suppressor of tan location: 3-26. origin: Spontaneous. discoverer: Bridges, 22k2. phenotype: Converts t to wild type. RK3. # su(tu-bw): suppressor of tumor with brown location: 3- (not located but probably in 3L). origin: Naturally occurring allele. discoverer: Glass, 1941. references: Glass and Plaine, 1952, Proc. Nat. Acad. Sci. USA 38: 697-705. Glass, 1954, DIS 28: 74. Burnet and Sang, 1964, Genetics 49: 223-35, 599-610. phenotype: Reduces incidence of melanotic masses in tu-bw homozygote from 85-100% in su(tu-bw)/+ to 5-10% in su(tu-bw) homozygote. Suboptimal ratios of pentose nucleotides, cholesterol deficiency, or excess L-tryptophan in the larval diet, as well as X irradiation of embryos, increase incidence of melanotic masses in tu-bw; su(tu-bw) homozygote. Glass and colleagues attribute this to an effect on su(tu-bw), whereas Burnet and Sang believe the reaction controlled by tu-bw is affected. Does not suppress tu-48 (Burnett, 1966, DIS 41: 161). RK3. # Su(var): Suppressor of variegation A series of dominant suppressors of variegation, mostly selected on the basis of their ability to suppress the mottling of In(1)wm4; where they have been tested, these mutations suppress variegated type position effects involving other loci as well. Two groups have performed extensive mutagenesis experiments, but there has apparently been no exchange of material nor any attempt to determine allelic relationships between the two samples of mutants. The Canadian group has designated its mutants as a Su(var)200 series for second- chromosome mutations and a Su(var)300 series for third- chromosome mutations. The German group uses Su-var(3)1, etc. to designate a series of suppressors on the third chromosome; we reconcile these terminologies but keep them separate by altering the second nomenclature to Su(var)3-1, etc. Despite the fact that some mutants from the two groups map to virtually identical positions, we choose to list them separately until appropriate complementation tests are performed. Most of these suppressors appear to be loss of function mutations and are frequently associated with deficiencies; in addition variega- tion suppression is often produced by heterozygous deficiencies for their loci. Of these, several have been shown to enhance variegation when duplicated (Tartof, Bishop, Jones, Hobbs, and Locke, 1989, Dev. Genet. (Amsterdam) 10: 162-76). genetic cytological locus location location ref ( comments | _____________________________________________________________________________________ Su(var) 3-41.3 70 10,11 viable Su(var)2-1 2-40.5 31A2-C1 1,4,14 butyrate sensitive; female sterile; 12 alleles Su(var)2-2 2-79.8 14 lethal Su(var)2-3 2-29.7 14 lethal Su(var)2-4 / 2-7.6 23A3-D4 7,14 lethal Su(var)2-5 2-31.1 28F2-29A1 14 lethal; 6 alleles; allelic to Su(var)205; triplo-enhancer Su(var)2-7 2-38.2 14 viable; fertile Su(var)2-8 2-13.0 24F7-25A1 7,12,14 lethal Su(var)2-9 2.44.8 14 female sterile Su(var)2-10 2-57.6 8,14 Su(var)2-11 2-45.7 14 female sterile Su(var)2-12 2-37.0 14 lethal Su(var)2-13 2-38.8 31A2-C1 14 viable; fertile Su(var)2-37 8 Su(var)2-57 8 Su(var)2-142 8 Su(var)2-144 8 Su(var)2-147 8 Su(var)201 2-40.1 9 lethal Su(var)205 2-28.9 29A 2, 9 lethal; allelic to Su(var)2-5; triplo-enhancer Su(var)206 2-51.3 9 lethal Su(var)207 2-32.0 9 lethal Su(var)209 2-35.4 9 viable Su(var)210 2-32.6 9 lethal Su(var)213 2-32.9 9 lethal Su(var)215 2-32.9 9 lethal Su(var)3-1 3-31.4 5,14 viable; fertile; 6 alleles Su(var)3-2 3-43.8 5,14 viable; fertile; 3 alleles Su(var)3-3 3-46.6 5,14 semilethal; female sterile; butyrate sensitive; 26 alleles Su(var)3-4 3-47.7 84D13-E2 5,14 lethal; 6 alleles Su(var)3-5 3-{50} 86B 5 butyrate sensitive; semilethal; sterile; T(2;3)58B;86B Su(var)3-6 3-51.1 87B4-7 5,6,14 lethal; 3 alleles Su(var)3-7 3-{53} 87E4-5 3,5,6,14 lethal; T(Y:3)87E1-2; triplo-enhancer Su(var)3-8 3-53.5 5,14 lethal; 2 alleles Su(var)3-9 3-56.4 5,14 viable; fertile; 4 alleles; triplo-enhancer Su(var)3-10 3-61.7 5,14 lethal; 2 alleles Su(var)3-11 3-76.4 94D-95A3 5 Minute Su(var)3-12 3-100.2 100F3-5 5 Minute Su(var)3-13 3-{53} 86F4-7 5,6,14 lethal Su(var)3-14 3-{50} 86C-D 5,6,14 lethal Su(var)302 3-62.4 9 viable Su(var)306 3-61.1 9 viable Su(var)309 3-56.4 88D 5, 9, 13 viable Su(var)314 3-60.8 9 viable Su(var)316 3-47.4 9 viable Su(var)319 3-48.6 9 viable Su(var)320 3-59.9 9 viable Su(var)323 3-47.3 9 viable Su(var)325 3-53.3 9 viable Su(var)326 3-left end 9 lethal Su(var)327 3-55.5 9 viable Su(var)328 3-left end 9 lethal Su(var)330 3-54.7 9 viable ( 1 = Dorn, Heymann, Lindigkeit, and Reuter, 1986, Chromosoma 93: 398-403; 2 = James and Elgin, 1986, Mol. Cell. Biol. 6: 3862-72; 3 = Henikoff, 1979, Genetics 93: 105-15; 4 = Reuter, Dorn, and Hoffmann, 1982, Mol. Gen. Genet. 188: 480-85; 5 = Reuter, Dorn, Wustmann, Friede, and Rauh, 1986, Mol. Gen. Genet. 202: 481-87; 6 = Reuter, Gausz, Gyurkovics, Friede, Bang, Spierer, Hall, and Spierer, 1987, Mol. Gen. Genet. 210: 429-36; 7 = Reuter and Szidonya, 1983, Chromosoma 88: 277-85; 8 = Reuter and Wolff, 1981, Mol. Gen. Genet. 182: 516-19; 9 = Sinclair, Mottus, and Grigliatti, 1983, Mol. Gen. Genet. 191: 326-33; 10 = Spofford, 1967, Genetics 57: 751-56; 11 = Spofford, 1969, Genetics 62: 555-71; 12 = Szidonya and Reuter, 1988, Genet. Res. 51: 197-208; 13 = Tartof, Bishop, Jones, Hobbs, and Locke, 1989, Dev. Genet. 10: 162-76; 14 = Wustmann, Szidonya, Tau- bert, and Reuter, 1989, Mol. Gen. Genet. 217: 520-27. | Phenotypes listed refer to homozygotes. / Synonym: Su(var)b5401. other information: In addition to the tabulated mutations, deficiencies for 31C-32A, 38C6-D1, 47E3-48A6, 86C-D, and 99B-D and duplications for 26B, 33C-34A, 57D-58A, and 99C-D shown to suppress variegation of In(1)wm4 (Wustmann, Szidonya, Taubert, and Reuter, 1989, Mol. Gen. Genet. 217: 520-27). phenotype: Reduces variegated mutant effect (sometimes com- pletely) of w, rst, fa, spl, nd, and dm in Dp(1;3)N264-58. Also reduces w variegation of In(1)wm4, rst variegation of In(1)rst3, and sc variegation of In(1)sc8. Enhances sc varie- gation of In(1)sc4 and y variegation of In(1)y3P. Semidom- inant; heterozygote less suppressed than homozygote. Shows maternal effect; Su(var)/+ offspring of Su(var)/Su(var) more nearly normal than Su(var)/+ offspring of Su(var)/+ mothers. Homozygote fertility slightly reduced. Viability excellent. RK2. # Su(var)2-1 phenotype: Su(var)2-1/+ but not Su(var)2-1/+/+ display nearly normal amounts of eye pigment in In(1)wm4 flies. Homozygous viable; females sterile; do not produce eggs. Survival reduced by the presence of the Y chromosome or by administra- tion of sodium n-butyrate, an inhibitor of histone deacetyla- tion (Reuter, Dorn, and Hoffmann, 1982, Mol. Gen. Genet. 188: 480-85). Exhibits significant hyperacetylation of histone H4 and increased accessibility of chromatin to endogenous nuclease, suggesting a defect in chromosome conden- sation (Dorn, Heymann, Lindigkeit, and Reuter, 1986, Chromo- soma 93: 398-403). alleles: Five alleles defining two complementation groups. allele origin comments ___________________________________________________ Su(var)2-11 spont noncomplementing Su(var)2-12 EMS complements Su(var)2-13 Su(var)2-13 X ray complements Su(var)2-12 and Su(var)2-14 Su(var)2-14 EMS complements Su(var)2-13 Su(var)2-15 X ray noncomplementing # Su(var)205 origin: Induced by ethyl methanesulfonate. synonym: E(var)29A. phenotype: Encodes a nonhistone chromosomal protein, HP1, which by immunofluorescent staining of polytene chromosomes with a monoclonal antibody, is localized to (, |, and intercallary heterochromatin as well as chromosome 4 (James and Elgin, 1986, Mol. Cell. Biol. 6: 3862-72). cytology: Placed in 29A by in situ hybridization. molecular biology: Sequence isolated from an expression library; hybridizes to a broad band in polytene subdivision 29A. In Northern blots the sequence recognizes an abundant 1.2 kb RNA; furthermore an aberrant transcript is seen in Su(var)205-bearing flies; attributable to missplicing caused by G -> A transition at the first nucleotide of the last intron (Eissenberg, James, Foster-Hartnett, Hartnett, Ngan, and Elgin, 1990, Proc. Nat. Acad. Sci. USA, 87: 9923-27). Su(var)2-54, an allele of Su(var)205, shown to contain a non- sense mutation in the gene encoding HP1 (Eissenberg, Hartnett, and Reuter). The conceptual amino acid sequence specifies a 18,101 dalton hydrophilic polypeptide; basic-to-acidic amino acid ratio of 1.2; has a run of six glutamic acid residues in a row in a putative (-helical stretch. No apparent similarity to published amino acid sequences (James and Elgin). other information: Duplications for the locus cause enhancement of variegation (Tartof, Bishop, Jones, Hobbs, and Locke, 1989, Dev. Genet. (Amsterdam) 10: 162-76). # Su(var)210 origin: Induced by ethyl methanesulfonate. alleles: Three alleles by complementation testing of lethal mutations: Su(var)2101, Su(var)2102, and Su(var)2103 recovered as Su(var)210, Su(var)214, and Su(var)216, respectively. # Su(var)3-1 alleles: Six ethyl methanesulfonate-induced alleles, Su(var)2- 11 to Su(var)2-16. # Su(var)3-2 alleles: Three alleles: Su(var)3-21 and Su(var)3-22 induced by ethyl methanesulfonate; Su(var)3-23 by X rays. # Su(var)3-3 location: 3-46.6 (on 3L based on its absence from induced C(3R)RM derivatives of Su(var)3-3-bearing chromosomes). phenotype: Homozygotes strongly semilethal in males; weakly so in females; homozygous females sterile; produce no eggs. Homozygous males have spread-wing phenotype and reduced fer- tility. Survival sensitive to the presence of the Y chromo- some as well as to the presence of 0.1 M butyrate in the medium. alleles: Twenty-five alleles: Su(var)3-313, Su(var)3-318, and Su(var)3-319 induced by X rays; the remainder by ethyl methanesulfonate. # Su(var)3-4 alleles: Six alleles: Su(var)3-41, and Su(var)3-46 induced by X rays; the remainder by ethyl methanesulfonate. # Su(var)3-5 origin: X ray induced. phenotype: Homozygotes strongly semilethal in males; weakly so in females; homozygous females sterile; produce no eggs. Homozygous males have reduced fertility. Survival sensitive to the presence of the Y chromosome as well as to the presence of 0.1 M butyrate in the medium. # Su(var)3-6 alleles: Three alleles: Su(var)3-61 ethyl methanesulfonate induced with normal cytology, Su(var)3-62 X ray induced, asso- ciated with T(Y;3)15 = T(Y;3)87B5-7, and Su(var)3-63 X ray induced, associated with Df(3R)Su-var6 = Df(3R)87B1-2;87D9-11. Su(var)3-61 shows some reduction in viability in trans heterozygotes with some alleles of l(3)87Bg; in one case a clear maternal effect is noted. cytology: Placed in 87B5-10 based on its inclusion in Df(3R)E079 = Df(3R)86F1-2;87B8-10 but not Df(3R)TE45 = Df(3R)86F1-2;87B5-6. # Su(var)3-7 origin: X ray induced. cytology: Identified by virtue of the variegation suppression of T(Y;3)409 = T(Y;3)87E2-5. Located between Ace and l(3)87Ee as indicated by its survival in combination with Df(3R)ry1607 = Df(3R)87D4-6;87E1-2 but not Df(3R)N42 = Df(3R)?;87E3-4 or Df(3R)N78 = Df(3R)?;87E3-4, the latter two deficiencies them- selves suppressing variegation. Corresponds to the dominant suppressor function identified by Henikoff (1979, Genetics 93: 105-15) by deficiency analysis. Duplication for the locus causes enhancement of variegation (Wustmann, Szidonya, Taubert, and Reuter, 1989, Mol. Gen. Genet. 217: 520-27). alleles: Complements all lethals in the region except Acej41; Acej41 has a weak dominant variegation-suppression effect. molecular biology: Genomic clone identified by transformation (Reuter, Giarre, Farah, Gausz, Spierer, and Spierer, 1990, Nature 344: 219-23). The sequence located in region 59-63 on chromosomal walk of Bender, Spierer, and Hogness (1983, J. Mol. Biol. 186: 17-33). cDNA clones isolated with transform- ing genomic clone sequenced; conceptual polypeptide has 932 amino acids with five widely separated zinc fingers, from 40- 107 residues apart in the N-terminal half of the protein. The regions between and around the fingers are rich in acidic residues. # Su(var)3-8 phenotype: Homozygous lethal. One allele temperature sensi- tive; dies at 25 but not at 18; homozygous flies raised at 18, nevertheless, exhibit some suppression of position-effect variegation. Homozygous females sterile; lay eggs that fail to hatch. alleles: Two ethyl methanesulfonate-induced alleles: Su(var)3-82 temperature sensitive. # Su(var)3-9 alleles: Thirteen alleles: Su(var)3-97 induced by X rays; the remainder by ethyl methanesulfonate. other information: Duplications for the locus cause enhancement of variegation (Tartof, Bishop, Jones, Hobbs, and Locke, 1989, Dev. Genet. (Amsterdam) 10: 162-76). # Su(var)3-11 origin: X ray induced. cytology: Identified by virtue of its association with Df(3R)M95A = Df(3R)94D-95A3. M(3)95A2 does not suppress variegation, however. # Su(var)3-12 origin: X ray induced. cytology: Identified by virtue of its association with Df(3R)MSu2, which is deficient in the region 100F3-5. # Su(var)3-13 origin: Induced by ethyl methanesulfonate. phenotype: Heterozygote shows weak suppression of variegation; homozygote lethal. alleles: Fails to complement alleles of l(3)86Fc; however, l(3)86Fc4 and l(3)86Fc5 fail to suppress variegation. cytology: Placed in 86F4-7 based on its location between Df(3R)TE7 = Df(3R)86F1-2;86F4-5 and Df(3R)E229 = Df(3R)86F6- 7;87B1-2. # Su(var)3-14 cytology: Gene inferred from the suppression of variegation seen in Df(3R)cu = Df(3R)86C1-2;86D8 heterozygotes; no suppression observed in Df(3R)M86D = Df(3R)86D1-2;86D4 hetero- zygtoes. # su(ve): suppressor of veinlet location: 3- -0.1 (0.1 unit to the left of ru). origin: Spontaneous. discoverer: Curry, 37a. phenotype: At 19, suppression of ve is complete except tip of L2 occasionally missing. At 25, suppression only partial with some overlap into range of unsuppressed ve. At 19, su(ve)/+ partially suppresses ve. RK2. cytology: Not included in Df(3L)D = Df(3L)61E2-F1;61A4-6 from T(Y;2;3)D; therefore, probably located in 61A-E. # su(vg): suppressor of vestigial location: 3-98. origin: Spontaneous. references: David, Javellot, and Tauzet, 1970, DIS 45: 33. phenotype: Temperature-sensitive recessive suppressor of vg. Suppression partial at 25; wings and halteres intermediate in size between vg and +. Wings, halteres, and positions of scu- tellar bristles nearly normal in flies reared at 28 and above. Flies reared below 20 resemble vg alone. Slight effect of su(vg)/f on vg expression at 28. vg; su(vg) lethal above 30 and below 13; 30% mortality at 25. # su(wa): suppressor of apricot location: 1-0.1. references: Levis, O'Hare, and Rubin, 1984, Cell 38: 471-81. Zachar, Davison, Garza, and Bingham, 1985, Genetics 111: 495-515. Zachar, Garza, Chou, Goland, and Bingham, 1987, Mol. Cell. Biol. 7: 2498-2505. Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97. phenotype: Produces a darker, brownish eye color in wa flies. Suppresses wa, waM, wa59k1, and wa59k9 but not wa2, wa3, wa4, waR84h, ws10 or any other w allele tested by Green (1959, Heredity 13: 303-15). Enhances wa60a5 and wM. Seems to act on wa by promoting transcription through the copia element that is inserted into the second intron in the same orienta- tion as that of w; the level of a read-through transcript is elevated in su(wa) wa compared to wa. su(wa) is without effect on the phenotype of whd81b11, which has copia inserted at another position and in the opposite direction (Zachar et al., 1985). su(wa) also enhances the expression of a subset of alleles with gypsy inserts that are also enhanced by su(s) and suppressed by su(f) and e(we); it also enhances lz34 and lzk (Rutledge et al.). alleles: No bona fide amorphic alleles reported; however, Df(1)sta, which is deficient for su(wa) survives (Rayle and Hoar, 1969, DIS 44: 94). allele origin discoverer synonym ref ( comments __________________________________________________________________ su(wa)1 X ray Schultz, 1941 *su(wa)2 X ray Schultz, 1944 possibly In(1)1D;1E su(wa)3 spont Green su(wa)G 1 in In(1)sc8, y31d wa su(wa)4 EMS Rayle 3 su(wa)5 EMS Rayle 3 su(wa)6 EMS Rayle 3 su(wa)7 EMS su(wa)A12 5 su(wa)8 EMS su(wa)D5 5 su(wa)9 EMS su(wa)DM17 5 su(wa)10 EMS su(wa)SD10 5 su(wa)11 X ray su(wa)/44 5 su(wa)12 X ray su(wa)/107 5 su(wa)13 P su(wa)hd7 5 su(wa)14 EMS su(wa)hdM8 5 su(wa)15 Birchler su(wa)84i 2 su(wa)16 Rendahl su(wa)85g 2 su(wa)17 Jaffe su(wa)BJ 2 su(wa)18 EMS su(wa)20 4 ( 1 = Green, 1954, DIS 28: 74; 2 = Mount, Green, Rubin, 1988, Genetics 118: 221-34; 3 = Rayle, 1972, Genetics 71: s50; 4 = Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97; 5 = Zachar, Garza, Chou, Goland, and Bingham, 1987, Mol. Cell. Biol. 7: 2498-2505. cytology: Placed in 1E1-2 by Rayle (1972, Genetics 71: s50); transposed to chromosome 3 by Tp(1;3)sta = Tp(1;3)1D3- 1E1;2A;89B21-C4. molecular biology: Gene isolated by transposon tagging. Iden- tity of the su(wa) transcription unit confirmed by transforma- tion with a 6.2 kb fragment. Three overlapping mature tran- scripts of 3.5, 4.6, and 5.2 kb produced from the 6.2 kb region, the two larger ones drastically reduced in su(wa) animals. The transcripts produced at approximately the same level at all developmental stages, in all body parts, and in cultured Drosophila cells (Zachar et al., 1987). # Su(wa)B1 location: 1- (to the right of w). origin: Recovered from hybrid-dysgenic cross. references: Birchler, 1984, Genetics 107: s12. phenotype: Heterozygotes, homozygotes, and hemizygotes display increased levels of pigment in wa eyes. # Su(wa)B2 location: 2- (Just proximal to c). origin: Recovered from hybrid dysgenic cross. references: Birchler, 1984, Genetics 107: s12. phenotype: Homozygous lethal. In heterozygotes causes an approximately two-fold increase in pigmentation of w alleles with lesions in the coding region. Without effect on four alleles that are not dosage compensated or on wsp alleles, whose lesions are 5' to the w transcription unit. Duplica- tions for the locus reduce pigmentation of w alleles. # Su(wch): Suppressor of cherry location: 2-4.0. discoverer: Lewis. references: Rasmusen, 1970, Hereditas 65: 83-96. Rasmusen and Ljung, 1973, Hereditas 73: 71-84. phenotype: Homozygous lethal; in heterozygotes leads to increased levels of eye pigmentation in wch, we, and wa; heterozygotes exhibit increased courtship activity leading to mating advantage over wild type (Connally, Burnet, and Sewell, 1969, Evolution 23: 548-59). # su(wh): suppressor of white honey location: 3- (not mapped). references: Lee, 1972, DIS 48: 18-19. phenotype: In homozygous su(wh) flies pigmentation of wh increased to a bright cherry color; wa and wa4 show slight suppression. Without effect on w, wa, waM, wbl, wc, wcf, wcol, we, wi, wsat, and wt. # su(wsp): suppressor of white-spotted location: 1-0.16 (based on 19 y-w recombinants). discoverer: Gelbart. references: Chapman and Bingham, 1985, DIS 61: 48-49. Davison, Chapman, Wedeen, and Bingham, 1985, Genetics 110: 479-94. phenotype: Results in nearly wild-type pigmentation of wsp1, wsp2, wsp3, and wsp4, but not wsp81d5. No phenotypic effect seen on eight other tested w alleles. The lesions of the spotted alleles map 500 to 1000 base pairs 5' to the w tran- scription unit and are postulated to affect an enhancer sequence. The normal allele of su(wsp) is postulated to encode a repressor of this enhancing function; the combination of the repressor and defective enhancer produces the spotted phenotype; the mutant allele of su(wsp), lacking repressor function, results in the derepression of the defective enhanc- ers at the time of eye-pigment deposition, leading to increased pigmentation. wsp81d5, a molecular deletion extend- ing more 3' that the other wsp alleles is postulated to be insensitive to the presence or absence of repression owing to loss of the site of interaction between the su(wsp) gene pro- duct and the w locus. Adult transcription of all w alleles, including w+, markedly increased by su(wsp), apparently after pigment deposition, since with the exception of wsp alleles, eye color does not respond to su(wsp). The latter observation implies a second site of repressor binding specific to adult transcription. # Su-x4: see Su(sph) #*Su(y3P): Suppressor of yellow-3 of Patterson location: 3-90. origin: X ray induced. discoverer: Parker, 48h. synonym: su-y31e. references: 1950, DIS 24: 62. phenotype: Su(y3P)/+ suppresses y3P to about normal color, except that wings remain yellowish. y3P; Su(y3P)/Su(y3P) is darker than wild type but wings remain yellow. May be suppression of variegation since extra Y chromosomes also suppress y3P. No effect on y, y2, y2S, y3d, y4, y35a, or ytd. Homozygote has low viability and fertility; occasionally, wings held out from body. RK2. # Su(z)2: Suppressor 2 of zeste location: 2-67 (distal to vg; also distal to Psc). references: Kalisch and Rasmuson, 1974, Hereditas 78: 97-104. Persson, 1976, Hereditas 82: 111-20. Wu, Jones, Lasko, and Gelbart, 1989, Mol. Gen. Genet. 218: 559-64. Adler, Charlton, and Brunk, 1989, Dev. Genet. (Amsterdam) 10: 249-60. phenotype: Dominant suppressor of the yellow eye color associ- ated with the z1 mutation. Can be detected in homozygous z1 females and in males. Lethal in homozygous or hemizygous con- dition and in trans-allelic heterozygotes. Viability reduced in trans heterozygotes in some Psc/Su(z)2 combinations, lethal in others. Psc and Su(z)2 are both members of the Su(z)2 com- plex. alleles: allele origin discoverer synonym ref ( comments ______________________________________________________________________ Su(z)21 EMS Rasmuson Su(z)2 3, 4, zeste->red eyes 5, 6 Su(z)21.b7 X ray Wu 1 revertant of Su(z)21; 2 kb deletion at 5' end of transcription unit Su(z)21.b8 X ray Wu 1 revertant of Su(z)21 Su(z)24 X ray Gelbart Su(z)45 2, 4, zeste->orange-maroon 5, 6 eyes Su(z)25 / ray Wu 5, 6 zeste->yellow-orange eyes ( 1 = Adler, Charlton, and Brunk, 1989, Dev. Genet. 10: 249- 60; 2 = Gelbart, 1971, Doctoral dissertation, University of Wisconsin, Madison; 3 = Kalisch and Rasmuson, 1974, Heredi- tas 78: 97-104; 4 = Persson, 1976, Hereditas 82: 111-20; 5 = Wu, 1984, Doctoral dissertation, Harvard University, Cambridge; 6 = Wu, Jones, Lasko, and Gelbart, 1989, Mol. Gen. Genet. 218: 559-64. cytology: Placed in 49E-F on the basis of its inclusion in Df(2R)vg-B = Df(2R)49D3-4;49F15-50A2 and its exclusion from Df(2R)vg-C = Df(2R)49B2-3;49E7-F1 and Df(2R)vg-D = Df(2R)49C1-2;49E4-5 (Wu). molecular biology: Reported to be distal to and transcribed from left to right, divergently from Psc (Adler et al.). # Su(z)301: see E(z) # Su(z)302: see Scm # sub: subito (T. Schupbach) location: 2-86. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect lethal or female sterile; homozygous females lay eggs which show no visible signs of development when observed under transmitted light in a stereo microscope. These eggs are defective in fertilization or very early embryonic development. alleles: Two alleles, sub1 and sub2, isolated as PF and HM. cytology: Placed in 55A-F, since uncovered by Df(2R)PC4 = Df(2R)55A;55F. other information: sub2 females form rare syncytial-blastoderm embryos. # Succinic dehydrogenase: see Sdh # Sucr: Sucrase location: 2- {37}. references: Oliver and Williamson, 1979, Biochem. Genet. 17: 987-907. phenotype: Thought to be the structural gene for sucrase [EC 3.2.1.26], a 100 kilodalton protein. alleles: Thought to exist in two forms by isoelectric focusing. cytology: Placed in 31C-F by changes in enzyme levels associ- ated with segmental aneuploids. # sunburst: see psnb #*sup: superwith location: 3- (not located). discoverer: Morgan, 10k. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 35. phenotype: Trident pattern on thorax dark. RK3. # supact: suppressor activated location: 1-0.0 (near mul; separable from sc). origin: Spontaneous. references: Lee, 1970, Austr. J. Biol. Sci. 23: 645-55. phenotype: Recessive; bristle and eye abnormalities produced by over 95% of females that are homozygous for su(Hw)2. Abnor- malities include irregular pattern of missing bristles (scu- tellars, dorsocentrals, vertical, post-verticals, and ocel- lars) and small granulated eyes. Restricted to females; not influenced by gene dosage or the presence of the Y chromosome, since neither XY nor X0 males homozygous for su(Hw)2 are affected, nor are males with two doses of the supact region at the tip of the X. No effect of supact on flies raised at 30; females but not males raised at 18 show enhanced eye effect, but no bristle effect. # super sex combs: see sxc # Superabdominal: see Sab under BXC # Super-Bar: see BS3i # superwith: see sup # suppressor: see su( ) # Suppressor: see Su( ) # suppressor activated: see supact # Surf wings: see Srf